The present invention relates to implantable medical devices which deliver energy to cardiac tissue in an attempt to restore a normal sinus rhythm to a patient.
Tachycardia refers to any fast, abnormal rhythm of the heart which may be amenable to treatment by electrical discharges. One form of tachycardia is referred to as ventricular tachyarrhythmia (VTA). A common therapy for treating VTA is to implant a cardiac pacer/defibrillator in the patient, Cardiac pacers traditionally have been used to detect a slow heart rate and in response discharge electrical energy into the heart tissue at a faster pace which increases the heart rate. Pacing technology also can respond to the detection of arapid heart rate by producing rapid pacing which terminates the tachycardia and thereby causing the heart rate to return to normal. This present cardiac pacing technology is not specifically designed to reduce the occurrence of ventricular tachyarrhythmia, but rather to terminate the condition after it occurs.
However, rapid pacing techniques can accelerate and worsen the arrhythmias in some instances. As a consequence, cardiac pacers that treat rapid heart rates do so in conjunction with an implantable cardioverter defibrillator (ICD). The cardioverter defibrillator detects rapid ventricular tachyarrhythmias that do not respond to rapid pacing and employs cardioversion/defibrillation to terminate the arrhythmia.
Clinical studies have demonstrated that abrupt short to long changes in the ventricular cycle length often preceded and possibly precipitated ventricular tachyarrhythmia. The ventricular cycle length, i.e. the period between ventricular contractions, normally remains relatively constant and varies only gradually, even upon the commencement of strenuous exercise. However, occasionally a premature ventricular contraction occurs in the form of a spurious pulse from a muscle cell which disrupts the normal electrical pulse pattern in the heart. Because the heart tissue often does not recover from an early beat in time to conduct the next regular electrical pulse, the subsequent normal heartbeat does not occur. Thus, the heart undergoes very rapid beat followed by a significantly longer compensatory pause before a subsequent beat occurs. As a result, the heart is subjected to a very fast heart rate which quickly changes to a very slow rate. Such rapid rate change significantly intensifies dispersion of refractoriness in patients who already have other causes of increased dispersion of refractoriness, such as damaged ventricular myocardium from a myocardial infarction or cardiomyopathy. A premature ventricular contraction may facilitate tachyarrhythmia in these patients.